FB2026_02 , released June 18, 2026
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Citation
Tang, M., Yuan, W., Bodmer, R., Wu, X., Ocorr, K. (2014). The role of Pygopus in the differentiation of intracardiac valves in Drosophila.  genesis 52(1): 19--28.
FlyBase ID
FBrf0223948
Publication Type
Research paper
Abstract
Cardiac valves serve an important function; they support unidirectional blood flow and prevent blood regurgitation. Wnt signaling plays an important role in the formation of mouse cardiac valves and cardiac valve proliferation in Zebrafish, but identification of the specific signaling components involved has not been addressed systematically. Of the components involved in Wnt signal transduction, pygopus (pygo), first identified as a core component of Wnt signaling in Drosophila, has not yet to be investigated with respect to valve development and differentiation. Here, we take advantage of the Drosophila heart model to study the role of pygo in formation of valves between the cardiac chambers. We found that cardiac-specific pygo knockdown in the Drosophila heart causes dilation in the region of these cardiac valves, and their characteristic dense mesh of myofibrils does not form and resembles that of neighboring cardiomyocytes. In contrast, heart-specific knockdown of the transcription factors, arm/β-Cat, lgs/BCL9, or pan/TCF, which mediates canonical Wnt signal transduction, shows a much weaker valve differentiation defect. Double-heterozygous combinations of mutants for pygo and the Wnt-signaling components have no additional effect on heart function compared with pygo heterozygotes alone. These results are consistent with the idea that pygo functions independently of canonical Wnt signaling in the differentiation of the adult interchamber cardiac valves.
PubMed ID
PubMed Central ID
PMC4142678 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    genesis
    Title
    genesis
    Publication Year
    2000-
    ISBN/ISSN
    1526-954X 1526-968X
    Data From Reference
    Genes (3)
    Human Disease Models (1)